Figure 4.

NKA α1 alleviated UA induced mitochondrial dysfunction in cultured human PTECs. NKA α1 expression vector or siRNA was added to cells for 30 h to overexpress or inhibit NKA α1 before 48 h UA 100 μg ml⁻¹ stimulation. UA significantly reduced mitochondrial membrane potential (a, b), increased UCP2 expression (c), reduced mtDNA copies (d), and complex I (e) and V (I) activities. UA did not change complex II (f), III (g) and IV (h) activities. The NKA α1 expression vector alleviated mitochondrial dysfunction by increasing the mitochondrial membrane potential (a, b), reducing UCP2 expression (c), increasing mtDNA copies (d), as well as complex I (e) and V (i) activities. The NKA α1 expression vector exert no effect on complex II (f), III (g) and IV (h) activities. *P<0.05 vs Cont, **P<0.01 vs Cont, #P<0.05 vs UA, ##P<0.01 vs UA.